Ozone Exposure, Cardiopulmonary Health, and Obesity: A Substantive Review

Abstract

From 1999-2014, obesity prevalence increased among adults and youth. Obese individuals may be uniquely susceptible to the proinflammatory effects of ozone because obese humans and animals have been shown to experience a greater decline in lung function than normal-weight subjects. Obesity is independently associated with limitations in lung mechanics with increased ozone dose. However, few epidemiologic studies have examined the interaction between excess weight and ozone exposure among adults. Using PubMed keyword searches and reference lists, we reviewed epidemiologic evidence to identify potential response-modifying factors and determine if obese or overweight adults are at increased risk of ozone-related health effects. We initially identified 170 studies, of which seven studies met the criteria of examining the interaction of excess weight and ozone exposure on cardiopulmonary outcomes in adults, including four short-term ozone exposure studies in controlled laboratory settings and three community epidemiologic studies. In the studies identified, obesity was associated with decreased lung function and increased inflammatory mediators. Results were inconclusive about the effect modification when data were stratified by sex. Obese and overweight populations should be considered as candidate at-risk groups for epidemiologic studies of cardiopulmonary health related to air pollution exposures. Air pollution is a modifiable risk factor that may decrease lung function among obese individuals with implications for environmental and occupational health policy.

Figure 1

Obesity prevalence among adults has increased since the early 2000s in the U.S. based on Behavioral Risk Factor Surveillance System data.

Figure 2

Overview of ozone exposure and obesity on inflammation and oxidative stress in the lung. When the respiratory system is challenged by ozone (O₃), particulate matter (PM), allergens, or bacteria, cytokines generated in the lungs (TNF-α, IL-1β, and IL-6), and LPS from disseminated bacteria can enhance the production of proinflammatory mediators released systemically by adipose tissue. The augmentation of systemic inflammation in the obese can enhance pulmonary inflammatory responses by enhancing leukocyte recruitment, cytokine production, microvascular permeability, and edema, which could potentially increase airway obstruction in preexisting lung disease.